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  • 1
    In: Ophthalmology, Elsevier BV, Vol. 125, No. 7 ( 2018-07), p. 1054-1063
    Type of Medium: Online Resource
    ISSN: 0161-6420
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
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  • 2
    Online Resource
    Online Resource
    American Society for Microbiology ; 1979
    In:  Antimicrobial Agents and Chemotherapy Vol. 15, No. 4 ( 1979-04), p. 608-615
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 15, No. 4 ( 1979-04), p. 608-615
    Abstract: A nosocomial epidemic of multiply resistant (MR) Klebsiella pneumoniae characterized by resistance to gentamicin, tobramycin, kanamycin, cephalothin, chloramphenicol, and ampicillin occurred in a Veterans Administration hospital from 1975 to 1977. A total of 66 infected or colonized patients were observed in a 2-year period; there were 43 urinary tract infections, 13 wound or soft tissue infections, 8 pneumonias, and 6 patients with only asymptomatic stool colonization. Four patients had both pneumonia and a urinary tract infection. There were five secondary bacteremias. The majority of MR K. pneumoniae strains were type 30, but types 17, 21, and 23 and nontypable organisms were also recovered. Other gram-negative bacilli with the same antibiotic resistance pattern were isolated from 14 patients. Seven MR K. pneumoniae and three resistant Escherichia coli isolates were shown to transfer resistance to E. coli K-12. MR K. pneumoniae -infected patients were seriously ill, had long hospitalization times (mean, 67 days), and were in close geographic proximity to other cases. Compared with controls, cases more frequently had prior antibiotic treatment and urinary catheters, but not respiratory instrumentation, nasogastric tubes, or antacid treatment. The apparent source of the outbreak was traced to an index case who entered the hospital with an MR K. pneumoniae urinary tract infection. Asymptomatic gastrointestinal carriage without infection elsewhere was infrequent (1.6% of cultured patients), but 78% of patients with MR K. pneumoniae infections at other sites also had the organism in their stools. Hospital antibiotic usage was unchanged before and during the outbreak. The identification of an index case and relative lack of asymptomatic stool carriers are unique features of this plasmid-mediated MR K. pneumoniae epidemic. Although this MR K. pneumoniae outbreak appeared to be controlled by the use of isolation techniques, a simultaneous increase in gentamicin resistance among other gram-negative organisms was observed.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1979
    detail.hit.zdb_id: 1496156-8
    SSG: 12
    SSG: 15,3
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  • 3
    Online Resource
    Online Resource
    Proceedings of the National Academy of Sciences ; 1972
    In:  Proceedings of the National Academy of Sciences Vol. 69, No. 8 ( 1972-08), p. 2219-2223
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 69, No. 8 ( 1972-08), p. 2219-2223
    Abstract: Biotin independence in E. coli requires five closely linked genes, bioA, bioB, bioF, bioC , and bioD . The residual gene activity of deletion mutants has been studied by complementation and enzyme assays. Deletion of the left end of the bioA gene does not impair expression of the remaining genes, but deletions from the left extending into bioB abolish all gene expression. Nonsense mutations in bioB reduce expression of bioC, bioF , and bioD . Therefore, the four genes, bioB, bioF, bioC , and bioD , are transcribed as a unit from left to right, from a promotor located between bioA and bioB . Expression of the bio genes is repressible by added biotin. Deletions removing the left end of bioA do not affect repressibility of bioD . Therefore the operator, as well as the promoter, lie to the right of bioA . One deletion that removes bioA, bioB , and bioF renders the bioD gene constitutive, presumably by fusion to an unknown operon. Therefore, the operator lies to the left of bioC .
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 1972
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    American Society for Microbiology ; 1974
    In:  Journal of Bacteriology Vol. 118, No. 1 ( 1974-04), p. 121-128
    In: Journal of Bacteriology, American Society for Microbiology, Vol. 118, No. 1 ( 1974-04), p. 121-128
    Abstract: The structural genes involved in l -arabinose metabolism are regulated by the protein product of the araC gene. This protein functions as both an activator and repressor of enzyme synthesis in this gene complex. Using λ h80dara deoxyribonucleic acid in hybridization studies, we have shown that the ara operon, including structural genes araB, araA , and araD , is transcribed in the direction araB to araD and that initiation of transcription of these genes requires an active araC gene. The half-life of this message, approximately 3 min at 30 C, is the same in the presence or absence of the araC protein in the activator state. However, an unexplained 2-min lag in decay of ara messenger ribonucleic acid that does not occur in decay of lac messenger ribonucleic acid is observed. This lag period requires activated araC protein.
    Type of Medium: Online Resource
    ISSN: 0021-9193 , 1098-5530
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1974
    detail.hit.zdb_id: 1481988-0
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Wiley ; 1997
    In:  Cancer Vol. 80, No. 7 ( 1997-10-01), p. 1335-1347
    In: Cancer, Wiley, Vol. 80, No. 7 ( 1997-10-01), p. 1335-1347
    Type of Medium: Online Resource
    ISSN: 0008-543X , 1097-0142
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 1997
    detail.hit.zdb_id: 1479932-7
    detail.hit.zdb_id: 2599218-1
    detail.hit.zdb_id: 2594979-2
    detail.hit.zdb_id: 1429-1
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  • 6
    Online Resource
    Online Resource
    Informa UK Limited ; 1995
    In:  Hospital Practice Vol. 30, No. 11 ( 1995-11-15), p. 41-49
    In: Hospital Practice, Informa UK Limited, Vol. 30, No. 11 ( 1995-11-15), p. 41-49
    Type of Medium: Online Resource
    ISSN: 2154-8331 , 2377-1003
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 1995
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  • 7
    Online Resource
    Online Resource
    Elsevier BV ; 1974
    In:  Biochemical and Biophysical Research Communications Vol. 56, No. 3 ( 1974-02), p. 629-634
    In: Biochemical and Biophysical Research Communications, Elsevier BV, Vol. 56, No. 3 ( 1974-02), p. 629-634
    Type of Medium: Online Resource
    ISSN: 0006-291X
    RVK:
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1974
    detail.hit.zdb_id: 1461396-7
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    American Society for Microbiology ; 1979
    In:  Antimicrobial Agents and Chemotherapy Vol. 15, No. 4 ( 1979-04), p. 616-624
    In: Antimicrobial Agents and Chemotherapy, American Society for Microbiology, Vol. 15, No. 4 ( 1979-04), p. 616-624
    Abstract: Gentamicin resistance in Klebsiella pneumoniae involved in an outbreak at the Minneapolis Veterans Administration Hospital was due to a transmissible R plasmid. In addition to gentamicin, this plasmid conferred resistance to tobramycin, kanamycin, ampicillin, carbenicillin, cephalothin, chloramphenicol, and sulfathiazole. R plasmids which transferred this complex antibiogram were identified in several clinical isolates, including four different serotypes of K. pneumoniae, Escherichia coli, Enterobacter cloacae , and Proteus morganii . The covalently closed circular form of all R plasmids isolated had a sedimentation coefficient of 76S to 77S, corresponding to a molecular weight of 58 × 10 6 . The possibility that a single R plasmid was responsible for the dissemination of multiple drug resistance among all of these different clinical strains was examined by characterizing the plasmids by using Eco RI restriction endonuclease. The same 15 fragments were obtained from each of the 10 plasmids analyzed. Their molecular weights ranged from 4 × 10 5 to 11 × 10 6 . Thus, we conclude that each of the 10 plasmids present in the various clinical strains isolated from the hospital over a 7-month period originated from a common source and that R plasmid transfer was important in their spread.
    Type of Medium: Online Resource
    ISSN: 0066-4804 , 1098-6596
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1979
    detail.hit.zdb_id: 1496156-8
    SSG: 12
    SSG: 15,3
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  • 9
    Online Resource
    Online Resource
    American Society for Microbiology ; 1977
    In:  Infection and Immunity Vol. 16, No. 1 ( 1977-04), p. 280-292
    In: Infection and Immunity, American Society for Microbiology, Vol. 16, No. 1 ( 1977-04), p. 280-292
    Abstract: Spontaneous phage A25-resistant (A25 R ) mutants of group A streptococci, strain K56, were isolated. The mutant cultures were unable to adsorb phage particles and hyperproduced M protein. Trypsin-digested A25 R cells regained the ability to adsorb phage particles, but failed to become infectious centers. This failure indicated that the mutation created a double barrier to phage growth: (i) receptors were masked by M protein; (ii) irreversibly adsorbed phage were unable to multiply. Spontaneous variants of one A25 R mutant, shown to be M negative (M − ) by electron microscopy, serological tests, and sensitivity to phagocytosis, rapidly adsorbed phage and were able to become infectious centers. Therefore, it was concluded that the mutant phenotype, A25 R , arose by a single mutation and genes coding for this trait and M protein synthesis were either genetically linked, controlled by a common gene or were biochemically interdependent. The A25 R phenotype was unstable and, as expected for plasmid-coded properties, acridine orange induced segregation of this phenotype. The parental M + , A25-sensitive (A25 S ) cultures proved to be a mixed population. Infection at various multiplicities indicated that this culture was composed of phage A25 S cells and cells more resistant to infection. Morphological comparison of thin sections of A25 R and A25 S cells by electron microscopy demonstrated striking differences. The A25 R culture was composed entirely of cells uniformly covered with M protein, whereas the A25 S M + wild-type culture was a mixed population, the majority of cells devoid of M protein. Phagocytosis by human blood enriched the culture for the latter cell type, suggesting that differences in phage sensitivity in the wild-type culture were also determined by the presence or absence of M protein. Thus M protein can serve a dual function for the streptococcal cell by allowing it to avoid infection by bacteriophage and ingestion by human leukocytes.
    Type of Medium: Online Resource
    ISSN: 0019-9567 , 1098-5522
    RVK:
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1977
    detail.hit.zdb_id: 1483247-1
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  • 10
    Online Resource
    Online Resource
    American Society for Microbiology ; 1972
    In:  Journal of Bacteriology Vol. 112, No. 2 ( 1972-11), p. 830-839
    In: Journal of Bacteriology, American Society for Microbiology, Vol. 112, No. 2 ( 1972-11), p. 830-839
    Abstract: Genetic deletions that terminate within the cluster of genes needed for biotin biosynthesis in Escherichia coli have been isolated and mapped by transduction with phages lambda and P1. These deletions order the point mutations in each of the five genes. Mutations causing biotin dependence were incorporated into λ pbio transducing phages. New bio − mutations were induced by exposure of λ pbio particles to ultraviolet light. Tests of complementation between such bio − pbio particles and bio − mutant cells divide the bio − mutations into five cistrons: bioA, bioB, bioF, bioC , and bioD . Certain bioA and bioF mutations exhibit intragenic complementation, suggesting that these genes determine enzymes composed of identical subunits.
    Type of Medium: Online Resource
    ISSN: 0021-9193 , 1098-5530
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1972
    detail.hit.zdb_id: 1481988-0
    SSG: 12
    Location Call Number Limitation Availability
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